Pathophysiology and biochemical condition in multi-organ failure due to SARS –COV-2 attacks | Adamas University

Pathophysiology and biochemical condition in multi-organ failure due to SARS –COV-2 attacks

SARS-CoV-2

Pathophysiology and biochemical condition in multi-organ failure due to SARS –COV-2 attacks

Student Contributors: Ria Sen and Jibitesh Sarkar (BSc 3rd year Student, Department of Biochemistry

The primary organ infected by SARS-CoV 2 is the upper respiratory tract. COVID-19 is characterized by viral pneumonia symptoms anorexia, fever, sore throat, fatigue, dry cough, dyspnoea, malaise, muscle pain, nasal congestion or headache, lymphopenia, etc. Within one week of the incubation period the clinical symptoms become severe. Mostly it leads to acute respiratory distress syndrome or ARDS. However according to the worldwide case reports its time worried about comorbidities in COVID-19. It was reported that in several cases Covid-19 outbreak is highly influenced by multi-organ involvement.

Pulmonary embolism and cardiovascular damage

In Brescia, Italy, it was reported that a woman had a heart attack with a weak left ventricle that it could pump only 1/3 its regular amount of blood. However there was no blockage found in the heart. The disruption seems to extend to blood itself. It was further reported huge no of COVID-19 patients had blood clotting abnormally. Fragments of blood clot can and reach the lungs, blocking major arteries which are termed as pulmonary embolism, which could kill patients instantly. Clotted fragments from arteries can also accumulate in the brain, which can cause a stroke. Blood vessel constriction also resulted in infection. Many reports have shown that there have been ischemias in the digits of hand and leg which is a decrease in blood flow that causes swollen, digit pain, and tissue death.

Diabetic and high blood pressure patients face a higher risk of COVID19. With the available data at present it is quite difficult to understand exactly what causes cardiovascular damage. Venous thromboembolism (VTE) also found in COVID-19 patients. Heart and blood vessel linings are highly susceptible to viral attack as they are rich in ACE2 receptors. As a whole, if lungs are affected, then its effects can extend too many other different organs.

Renal failure:

According to reported data Acute Kidney Injury (AKI) is one of the major reasons for the higher mortality rate in Wuhan, China COVID-19 patients. Presence of protein and blood in patient urine reported in quite a high number (>40%) of infected folks. the scenario worsens when a minute fraction of the virus infects the kidney along with the lung. In electron microgram of the kidney from autopsies identified viral particles that suggest a direct viral attack. However, there is the possibility that the kidney damage can be collateral damage. The use of ventilators or antiviral drugs like remdesivir with experimental dosage may increase the risk of kidney damage. Cytokine storms can reduce the flow of blood to the kidney resulting in irreversible damage. Also the presence of different other comorbid situations like diabetes can magnify the risk of AKI.

Brain damage:

In addition to their presence in the lungs the ACE2 receptors are also present in the neural cortex and brain stem. Symptoms found in the COVID-19 patients also focuses on the brain and Central Nervous System(CNS). Due to the use of sedative and ventilator it is difficult to monitor the brain activity in a major population of the COVID-19 patients. Certain reports of the infected patients indicate having brain inflammation encephalitis, along with seizures, and “sympathetic storm,” (cytokine storm occurs in the brain). Viral infection causes oxygen starvation which reduces the brain stem reflex and finally leads to stroke. However, the underlying mechanism of brain penetration and receptor interaction by the virus is still unknown. Traces of the new virus have also been found in the cerebrospinal fluid (CSF) of an infected patient in Japan who was reported to later develop meningitis and encephalitis which suggests that it can invade the brain. But there are a lot of other factors that must be taken into consideration like a cytokine storm that causes brain swelling, and the blood’s exaggerated tendency to clot could trigger strokes. A possible way of entry into the human body can be via the nose then upward via the olfactory bulb which is connected with the brain. This possible route also explains the reason for the loss of smell in COVID-19 patients.

Gastrointestinal infection:

The abundant presence of the ACE2 receptor located in the outer epithelial lining of the lower digestive tract makes it vulnerable against SARS-COV2. Lots of COVID-19 patients are primarily developed symptoms of gastrointestinal infection (such as bloody diarrhea, vomiting, and abdominal pain) which turns positive for coronavirus. In around half of sampled patient stool samples viral RNA has been found. According to a report by a Chinese team, the protein shell of the virus was found in gastric cells, duodenal cells, and rectal cells in biopsies from a COVID-19 patient, raising the chances that it probably replicates in the gastrointestinal tract. GI infections are not on the list so if an individual has fever and diarrhea he/she won’t be tested for  COVID-19. Viral existence in the GI tract raises the possibility that it can be present in feces. However it’s unclear whether stool contains a live infectious virus, not just viral fragments. To date there is no strong evidence that fecal transmission is a high-risk factor and also its probability is very low.

The disease doesn’t stop at the intestine and marches further down the body. There have been reports of hospitalized patients developing conjunctivitis—pink, watery eyes but it is not definite whether the virus directly invades the eyes. Also, some reports suggest that more than half of the COVID-19 hospitalized had elevated levels of enzymes indicating liver injury or the bile ducts injury, but the liver injury is not caused due to direct viral invasion rather the application of drugs or an immune system working in overdrive is more likely driving the liver damage.

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